Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of alcoholism and liver disease on memory functioning in alcoholics were studied by comparing four groups: normal healthy controls, alcoholics without liver disease, alcoholics with biopsy-confirmed cirrhosis, and nonalcoholics with postnecrotic cirrhosis. Memory capacity was evaluated employing the Benton Visual Retention Test (BVRT), the Rey-Osterreith Complex Figure Test, Digit Span, and the Brown Peterson four-word short-term memory test. A 2 x 2 ANOVA revealed significant main effects for both alcohol and cirrhosis on Digits Forward and the total score on the Brown Peterson test. Additionally, there were significant main effects for cirrhosis on the BVRT. The Brown Peterson test was analyzed using a repeated measures 2 x 2 ANOVA. Significant effects for cirrhosis were observed at all three interpolation periods. The effects for alcohol approached significance at the 30-sec (most difficult) interpolation period. Analysis of error patterns on the Brown Peterson test indicated that overall omission errors were most commonly made among all groups. Significant effects were found for alcohol on omissions and intrusion, while the cirrhosis factor yielded significant effects for phonemic, perseverative, and omission errors. This study demonstrates the importance of liver disease underlying the etiology of memory impairments in alcoholics. The results confirm our earlier findings that neuropsychologic deficits seen in alcoholics may be the result of the combination of alcohol abuse and liver disease.
 ...
PMID:The role of cirrhosis in memory functioning of alcoholics. 178 89

The aim of this study was to assess serum zinc levels in a cohort of healthy subjects and cirrhotic patients from Mexico City. A total of 153 healthy subjects and 100 cirrhotic patients, males and females aged 18-65, were studied. Inclusion criteria for healthy subjects were (1) Mexican-born with first and second generation relatives born in Mexico, and (2) somatometric (body mass index under 30) and clinical evaluation establishing that they had no underlying disease. Entry criteria for cirrhotic patients were (1) clinical and histological proven cirrhosis, (2) compensated liver disease (absence of coma, bleeding hemorrhage or refractory ascitis), and (3) cirrhosis of any cause. Zinc serum levels were measured with atomic absorption spectrophotometry. In healthy subjects, mean serum levels were 77.4 +/- 4.2 micrograms/dl (range 42.9-105.2 micrograms/dl). In cirrhotic patients zinc serum levels (58.9 +/- 16.1 micrograms/dl, range 22-88 micrograms/dl) were significantly lower than in healthy subjects (p < 0.05). A stepwise decline in serum zinc with worsening Child class (A, 73.4 +/- 13; B, 64.4 +/- 12; C, 55.8 +/- 15.6; p < 0.05 by ANOVA test) was found. In conclusion, this study confirms that zinc serum levels are significantly lower in cirrhotic patients and shows that zinc serum levels in a cohort of 153 healthy subjects from Mexico City were unexpectedly lower compared to those found in other countries. This last finding might be explained by different dietetic patterns and deserves further investigation.
 ...
PMID:Serum zinc concentrations in two cohorts of 153 healthy subjects and 100 cirrhotic patients from Mexico City. 758 34

Arterial vasodilation is considered to be the key factor in the development of sodium and water retention leading to ascites formation in cirrhosis. To determine if nitric oxide (NO) is involved in the pathogenesis of arterial vasodilation in cirrhosis, we measured the concentration of cyclic guanosine monophosphate (cGMP), the second messenger of NO, in arterial tissue from rats with carbon tetrachloride-induced cirrhosis. Aortic cGMP concentration was markedly increased in cirrhotic rats, particularly in those with ascites (ascites, 826 +/- 70; no ascites, 597 +/- 48; controls, 331 +/- 25 fmol/mg, ANOVA F = 23.1, P < .0001), and correlated inversely with arterial pressure (r = -.56, P < .0001) and systemic vascular resistance (r = -.69, P = .014) and directly with cardiac index (r = .74, P < .01). The chronic administration of the NO synthesis inhibitor NG-nitro-L-arginine-methyl-ester (L-NAME) (10 mg/kg/day for 7 days) induced a marked reduction in aortic cGMP concentration in cirrhotic rats with ascites to similar values obtained in L-NAME-treated control rats (86 +/- 14 vs. 89 +/- 8 fmol/mg, respectively, NS), indicating that the high-aortic cGMP content in cirrhotic rats was caused by an increased NO synthesis. Mean arterial pressure after L-NAME treatment increased to similar values in both groups of animals. These results suggest that in cirrhosis there is an increased vascular production of NO that may play a role in the pathogenesis of arterial vasodilation.
 ...
PMID:Increased aortic cyclic guanosine monophosphate concentration in experimental cirrhosis in rats: evidence for a role of nitric oxide in the pathogenesis of arterial vasodilation in cirrhosis. 776 8

Portal hypertensive gastropathy is a major complication of cirrhosis. The aims of this study were to characterize portal vein hemodynamics and sympathetic nervous activity in cirrhotic patients with gastropathy. Forty-seven cirrhotics (mild gastropathy in 7) and 25 controls were included in this study. Portal vein hemodynamics was assessed by echo-Doppler, and sympathetic nervous activity by plasma adrenaline and noradrenaline concentrations. Portal blood flow was similar in cirrhotics and controls. However, the congestion index of the portal vein (calculated as the ratio of cross-sectional area and blood velocity) was significantly higher in the former than in the latter. Furthermore, the congestion index of the portal vein paralleled the severity of the gastropathy (ANOVA, p < 0.05). Plasma adrenaline and noradrenaline concentrations were higher in cirrhotics than in controls. However, there was no linear relationship between plasma adrenaline (ANOVA, NS) and noradrenaline (ANOVA, NS) concentrations and the severity of gastropathy. These results suggest a relative contribution of "passive congestion" in the pathogenesis of gastropathy.
 ...
PMID:Portal vein hemodynamics in cirrhotic patients with portal hypertensive gastropathy: an echo-Doppler study. 795 44

The influence of insulin on lipolysis and glucose metabolism in abdominal adipose tissue was studied in situ with the microdialysis technique during a euglycaemic insulin clamp (1 mU kg-1 min-1) in nine cirrhotic patients and 10 controls. The cirrhotic patients displayed a 50% decrease in glucose utilization rate during the clamp (P < 0.001). Dialysate glucose levels decreased similarly by 20-30%., in patients and controls, which in the presence of unchanged local blood flow in the adipose tissue in response to insulin, is at hand with a glucose uptake into the adipocytes of similar magnitude in both groups. Before and during the clamp, the arterial and dialysate levels of glycerol were higher in the patients than in the control subjects (ANOVA P = 0.001 and 0.048 in arterial blood and dialysate, respectively). In relative terms, however, insulin induced a 70% reduction of arterial and dialysate glycerol in both groups. The concentrations of lactate and pyruvate in the dialysate and blood increased in a similar way in both groups during hyperinsulinaemia. The results suggest an increased rate of lipolysis in cirrhotic patients. Insulin cannot lower it to normal, although it is still capable of achieving a relative reduction. No explanation was found in the adipose tissue to the insulin resistance to whole-body glucose utilization that was noted in the patients with cirrhosis.
 ...
PMID:Influence of insulin on glucose metabolism and lipolysis in adipose tissue in situ in patients with liver cirrhosis. 814 60

Chronic bile duct obstruction in the rat leads to biliary cirrhosis but maintained hepatocellular mass. We have previously demonstrated translocation of epidermal growth factor receptor to nuclei. It remained unclear, however, whether this was due to hepatocyte proliferation and/or altered handling of epidermal growth factor receptor. Therefore, in the present investigation we stereologically estimated expression of proliferating cell nuclear antigen, a marker of the S phase of teh cell cycle at 1, 2, 3, 7, 14, 21 and 28 days after bile duct ligation. Proliferating cell nuclear antigen positive hepatocytes averaged 2.1 +/- 3.6% in sham-operated control animals. This increased to 20.7 +/- 6.4, 26.8 +/- 18.7, 31.3 +/- 23.9, 42.3 +/- 16.6 and 24.7 +/- 28.0% 3, 7, 14, 21 and 28 days after bile duct ligation, respectively (p<0.005 by ANOVA). This was correlated with the number of epidermal growth factor receptor positive nuclei (rs = 0.737) and inversely with the maximal binding capacity of epidermal growth factor to a crude plasma membrane fraction (rs = 0.697) reported previously. We conclude that bile duct ligation in the rat induces a significant hepatocellular proliferation as assessed by proliferating cell nuclear antigen expression and that this process could, at least in part, be related to increased nuclear expression of the epidermal growth factor receptor.
 ...
PMID:The overexpression of proliferating cell nuclear antigen in biliary cirrhosis in the rat and its relationship with epidermal growth factor receptor. 865 64

Acquired deficiencies of fibrinogen, antithrombin III and plasminogen are reported in liver disease, and it is known that their plasma levels fluctuate during the day. The aim of this study was to investigate the circadian rhythms of these three factors in chronic liver disease. Five groups of subjects were considered: (A) 15 healthy controls: (B) 15 patients with hepatic alcoholic steatosis; (C) 15 patients with chronic active hepatitis; (D) 15 patients with compensated cirrhosis of the liver, and (E) 15 patients with decompensated cirrhosis with ascites. The levels of fibrinogen, antithrombin III and plasminogen were determined in blood samples drawn in each subject during the span of a day every 3 h starting from midnight. The time-related values were analyzed using the 'population-mean cosinor' method. Groups A and B presented a significant (p < 0.05) circadian rhythm for each variable, group C a significant (p < 0.05) circadian rhythm for fibrinogen and antithrombin III and groups D and E no significant (p > 0.05) circadian rhythms. Statistically significant differences (p < 0.05) were demonstrated among the groups in the mean daily levels of the three variables by ANOVA, the concentrations decreasing with disease severity. These data confirm the existence of a significant diurnal periodicity in the circulating levels of fibrinogen, antithrombin III and plasminogen in controls and suggest that liver disease is associated with progressive circadian modifications in the temporal structure of fibrinogen, antithrombin III and plasminogen, related to the stage of the liver disease. The rhythm derangements may be considered markers of evolution in liver disease.
 ...
PMID:Circadian rhythms of fibrinogen antithrombin III and plasminogen in chronic liver diseases of increasing severity. 930 31

Polyenylphosphatidylcholine (PPC), a polyunsaturated phospholipid extract from soy beans, prevents the development of liver cirrhosis in animal models. Its mechanism of action is unknown. Based on the hypothesis that PPC might act by decreasing hepatic stellate cell proliferation, we studied the effect of PPC and its main components, dilinoleoylphosphatidylcholine (DLPC) and palmitoyl-linoleoylphosphatidylcholine (PLPC), on PDGF-induced stellate cell proliferation and intracellular signal transduction. Normal rat hepatic stellate cells in tissue culture were serumstarved, and incubated with 10ng/ml PDGF in the absence or presence of phospholipids. Cell proliferation was measured by 3H-thymidine incorporation. P44MAPK activation was determined by kinase assay, and AP-1 binding by electrophoretic mobility shift assay. PPC (200 ng/ml) significantly inhibited PDGF-induced proliferation (p < 0.05; ANOVA, n = 3) and antagonized PDGF-induced P44MAPK activation and AP-1 binding. This effect was mimicked by DLPC but not by PLPC. Neither DLPC nor PLPC prevented PDGF receptor activation. We conclude that PPC exerts a previously unrecognized effect on mitogen-induced stellate cell proliferation which may be mediated by DLPC. Inhibition of this cascade represents a potential mechanism for the inhibitory effect of PPC on hepatic fibrogenesis.
 ...
PMID:Polyenylphosphatidylcholine inhibits PDGF-induced proliferation in rat hepatic stellate cells. 967 6

Plasma fibronectin was determined in 29 patients with decompensated cirrhosis (7 patients had bacterial infection) and 23 patients with malignant liver disease. The obtained values were compared with the fibronectin values in 20 healthy subjects belonging to the control group in order to determine the possible diagnostic value of this dimer glycoprotein of high molecular weight whose role in the organism has not been completely explained. Fibronectin was determined on nephelometer with the use of specific antiserum by Behringwerke. The results expressed as mean values and SD were compared with monofactorial variance analysis (method One-way ANOVA). Fibronectin values in patients with liver cirrhosis were statistically significantly lower than in the control group (p < 0.01), which is also the case with correlation with malignant liver disease (p < 0.01). The fibronectin values in patients with malignant diseases were almost the same as the control group values (p < 0.01). In 7 patients with liver cirrhosis and bacterial infection the fibronectin values were statistically significantly higher in relation to those in the remaining 22 patients with cirrhosis but without bacterial infection (p < 0.001). The investigation in this study indicated that the decrease of mean fibronectin values is related to hepatic failure which is of diagnostic value, while normal values in malignant diseases do not favor the opinion on fibronectin as a tumor marker. Higher fibronectin values in infection in patients with liver cirrhosis are not clear, which indicated the total complexity of the relation between fibronectin as a dimer glycoprotein and chronic liver diseases including malignant.
 ...
PMID:[Diagnostic importance of fibronectin in chronic liver diseases]. 1035 2

Implication of serum atrial natriuretic peptide (ANP) and endothelin-1 (ET1) in the central nervous system (CNS)-induced natriuresis and hypertension respectively, was investigated in healthy and cirrhotic rats. Both healthy and nonascitic CCl(4)-induced cirrhotic rats under pentobarbital anesthesia received either normotonic (140 mmol/L) or hypertonic (320 mmol/L) NaCl artificial cerebrospinal fluid into the CNS lateral ventricle at a rate of 8.3 microl/min for 120 min. A sham operated group, but not centrally infused, served as matched control. Hypertonic NaCl solution significantly increased mean arterial pressure (MAP) similarly in both healthy (n = 5) ((MAP: 16 mm Hg, 13%) and cirrhotic rats (n = 6) ((MAP: 20 mm Hg, 15%) (ANOVA, p <.001) although the latter showed a slower increment. Under hypertonic NaCl infusion, natriuresis was also significantly increased in a similar manner in both healthy (U (Na) V: baseline: 0.38 +/- 0.22 micromol/min x 100 g; experiment: 2.36 +/- 0.90 micromol/min x 100 g; mean +/- SD) and cirrhotic rats (0.69 +/- 0.48 vs. 3.16 +/- 0.87; p <.001). By contrast, central hypertonic NaCl solutions did not show a significant modification of serum ANP in neither healthy (62 +/- 18 fmol/ml vs. 51 +/- 17 fmol/ml) nor cirrhotic rats (126 +/- 61 vs. 115 +/- 30). Likewise, ET-1 was not significantly modified under central hypertonic NaCl infusion in neither healthy (352 +/- 46 pg/ml vs. 344 +/- 39 pg/ml) nor cirrhotic rats (287 +/- 58 vs. 277 +/- 61). Despite no modification in serum ANP, there was a significant increment in urinary excretion of cGMP under central hypertonic NaCl infusions in bo th healthy (6.8 +/- 4.1 pmol/min x 100 g vs. 13.0 +/- 6.5 pmol/min x 100 g; p <.05) and cirrhotic rats (8.6 +/- 1.7 vs. 11.1 +/- 1.3; p <.05). Our data indicate the preservation of the mechanisms of central natriuresis in a model of non-ascitic CCl(4 )-induced cirrhosis in rats. An increment in urinary cGMP could potentially be implicated in the natriuretic response obtained by intracerebroventricular hypertonic NaCl stimulus in both healthy and cirrhotic rats. The lack of modification of serum ANP and ET-1 does not appear to support a systemic implication of these peptides in the natriuretic and hypertensive responses respectively induced by this manoeuvre.
 ...
PMID:Intracerebroventricular infusion of hypertonic NaCl increases urinary CGMP in healthy and cirrhotic rats. 1077 28


1 2 3 4 5 Next >>